Foam cell
Foam cells are fat-laden macrophages seen in atherosclerosis.[1][2] They are an indication of plaque build-up, or atherosclerosis, which is commonly associated with increased risk of heart attack and stroke.
Foam cells are formed when the body sends macrophages to the location of a fatty deposit on the blood vessel walls.[3] The macrophage surrounds the fatty material in an attempt to destroy it. The cell becomes filled with lipids (fats). The lipids surrounded by the macrophage give it a “foamy” appearance.
In chronic hyperlipidemia, lipoproteins aggregate within the intima of blood vessels and become oxidized by the action of oxygen free radicals generated either by macrophages or endothelial cells. The macrophages engulf oxidized low-density lipoproteins (LDLs) by endocytosis via scavenger receptors, which are distinct from LDL receptors. The oxidized LDL accumulates in the macrophages and other phagocytes, which are then known as foam cells.[4] Foam cells form the fatty streaks of the plaques of atheroma in the tunica intima of arteries.
Low-density lipoprotein (LDL) cholesterol is contained by a foam cell. LDL is also known as “bad” cholesterol. It becomes a marker for atherosclerosis. Foam cells are the body’s way of trying to get rid of bad cholesterol from the blood vessels. Foam cells do not give off any explicit signs or symptoms, but they are part of the origin of atherosclerosis. Foam cells are very small in size and can only be truly detected by examining a fatty plaque under a microscope after it is removed from the body. HDL cholesterol is good cholesterol and it removes harmful bad cholesterol from where it does not belong.[5]
Foam cells are not dangerous as such, but can become a problem when they accumulate at particular foci thus creating a necrotic centre of atherosclerosis. If the fibrous cap that prevents the necrotic centre from spilling into the lumen of a vessel ruptures, a thrombus can form which can lead to emboli occluding smaller vessels. The occlusion of small vessels results in ischemia, and contributes to stroke and myocardial infarction, two of the leading causes of cardiovascular-related death.
Atherosclerosis is the hardening and narrowing of the arteries, due to the formation of plaques in the blood vessel. Atherosclerosis is the usual cause of heart attacks, strokes, and peripheral vascular disease. Together, these diseases are called “cardiovascular disease.” [6]
Foam Cells will form around silicone breast implants as well.[7]
Autoimmunity occurs when the body starts attacking itself. The link between atherosclerosis and autoimmunity is plasmacytoid dendritic cells (pDCs). PDCs contribute to the early stages of the formation of atherosclerotic lesions in the blood vessels. Stimulation of pDCs leads to an increase of macrophages present in plaques.
References
- ^ Hotamisligil GS (2010). "Endoplasmic reticulum stress and atherosclerosis". Nature Medicine. 16 (4): 396–399. doi:10.1038/nm0410-396. PMC 2897068. PMID 20376052.
- ^ Oh J, Riek AE, Weng S, Petty M, Kim D, Colonna M, Cella M, Bernal-Mizrachi C (2012). "Endoplasmic reticulum stress controls M2 macrophage differentiation and foam cell formation". Journal of Biological Chemistry. 287 (15): 11629–41. doi:10.1074/jbc.M111.338673. PMC 3320912. PMID 22356914.
{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link) - ^ Manning, Robert. "Livestrong.com". What Is A Foam Cell?. Demand Media Inc. Retrieved 5 March 2013.
- ^ Kumar, Abbas, Fausto, Aster (2010). "11". Robbins and Cotran: Pathologic Basis of Disease (Eighth Edition International ed.). Philadelphia: Saunders Elsevier. pp. 500–501. ISBN 978-1-4160-3121-5.
{{cite book}}: CS1 maint: multiple names: authors list (link) - ^ Maddox, Thomas. "WebMD". Cholesterol & Triglycerides Health Center. WebMD LLC. Retrieved 19 March 2013.
- ^ Berkerman, James. "WebMD". Heart Disease Health Center. WebMD LLC. Retrieved 18 March 2013.
- ^ van Diest, P J; Beekman, W H; Hage, J J (1998). "Pathology of silicone leakage from breast implants". Journal of Clinical Pathology. 51 (7): 493–497. PMC 500799.